OBJECTIVES/HYPOTHESIS: To determine if a relationship exists between depression, disease severity, and sleepiness in patients with obstructive sleep apnea (OSA).STUDY DESIGN: Case control study.METHODS: Fifty-three consecutive patients with suspected OSA were evaluated before treatment and compared with controls by using the Beck Depression Inventory (BDI), Epworth Sleepiness Scale (ESS), and polysomnography.RESULTS: OSA was associated with an increased risk of depression in the study group compared to the control group (odds ratio = 6.3, 95% confidence interval: 1.9-20.6, P = .002); depression was seen in 35% of OSA patients and 8% of controls (P < .001). There was a significant correlation between BDI and ESS scores (r = 0.342, P = .012). In addition, ESS was significantly associated (P = .039) with depression in a linear regression model that controlled for race, sex, age, and respiratory disturbance index (RDI). RDI and depression were weakly associated (P = .056) in this model, and there was no correlation found between BDI scores and OSA disease severity (RDI)(r = 0.446).CONCLUSIONS: Patients with OSA and daytime sleepiness are more likely to have depressive symptoms as compared with controls. OSA disease severity, as measured with the RDI score, is a weak predictor of BDI score, and no correlation was seen between the severity of OSA and BDI scores after controlling for other factors. However, there was a strong correlation between sleepiness (ESS) and disease severity (BDI). These data suggest that OSA patients with symptoms of excessive sleepiness have the highest risk of associated depressive symptoms and may benefit most from depression screening. Laryngoscope, 2010.----Arch Ophthalmol. 2010 Oct;128(10):1257-63.

Proc Natl Acad Sci U S A. 2010 Oct 11. [Epub ahead of print]Light at night increases body mass by shifting the time of food intake.Fonken LK, Workman JL, Walton JC, Weil ZM, Morris JS, Haim A, Nelson RJ.Departments of Neuroscience and Psychology, Ohio State University, Columbus, OH 43210.AbstractThe global increase in the prevalence of obesity and metabolic disorders coincides with the increase of exposure to light at night (LAN) and shift work. Circadian regulation of energy homeostasis is controlled by an endogenous biological clock that is synchronized by light information. To promote optimal adaptive functioning, the circadian clock prepares individuals for predictable events such as food availability and sleep, and disruption of clock function causes circadian and metabolic disturbances. To determine whether a causal relationship exists between nighttime light exposure and obesity, we examined the effects of LAN on body mass in male mice. Mice housed in either bright (LL) or dim (DM) LAN have significantly increased body mass and reduced glucose tolerance compared with mice in a standard (LD) light/dark cycle, despite equivalent levels of caloric intake and total daily activity output. Furthermore, the timing of food consumption by DM and LL mice differs from that in LD mice. Nocturnal rodents typically eat substantially more food at night; however, DM mice consume 55.5% of their food during the light phase, as compared with 36.5% in LD mice. Restricting food consumption to the active phase in DM mice prevents body mass gain. These results suggest that low levels of light at night disrupt the timing of food intake and other metabolic signals, leading to excess weight gain. These data are relevant to the coincidence between increasing use of light at night and obesity in humans.----

Am J Respir Crit Care Med. 2010 Oct 8. [Epub ahead of print]Upper Airway Structure and Body Fat Composition in Obese Children with Obstructive Sleep Apnea Syndrome.Arens R, Sin S, Nandalike K, Rieder J, Khan UI, Freeman K, Wylie-Rosett J, Lipton ML, Wootton DM, McDonough JM, Shifteh K.Division of Respiratory and Sleep Medicine, The Children's Hospital at Montefiore, Montefiore Medical Center, and Albert Einstein College of Medicine, Bronx, New York, United States.AbstractRATIONALE: Mechanisms leading to OSAS in obese children are not well understood. The aim of the study was to determine anatomical risk factors associated with OSAS in obese children as compared to non-OSAS obese controls.METHODS: MRI was used to determine the size of upper airway structure, and body-fat composition. Paired analysis was used to compare between groups. Mixed effects regression models and conditional multiple logistic regression models were used to determine whether BMI Z-score was an effect modifier of each anatomic characteristic as it relates to OSAS.RESULTS: We studied 22 obese OSAS subjects (12.5±2.8 yrs, BMI Z-score: 2.4±0.4) and 22 obese controls (12.3±2.9 yrs, BMI Z-score: 2.3±0.3). As compared to controls, OSAS subjects had a smaller oropharynx (p<0.05), and larger adenoid (p<0.01), tonsils (p<0.05) and retropharyngeal nodes (p<0.05). The size of lymphoid tissues correlated with severity of OSAS while BMI Z-score did not have a modifier effect on these tissues. OSAS subjects demonstrated increased size of parapharyngeal fat-pads (p<0.05), and abdominal visceral fat (p<0.05). The size of these tissues did not correlate with severity of OSAS and BMI Z-score did not have a modifier effect on these tissues.CONCLUSIONS: Upper airway lymphoid hypertrophy is significant in obese children with OSAS. The lack of correlation of lymphoid tissue size with obesity suggests that this hypertrophy is caused by other mechanisms. Though the parapharyngeal fat-pads and abdominal visceral fat are larger in obese children with OSAS we could not find a direct association with severity of OSAS or with obesity.